Purpose To determine the levels of Th17-associated cytokines, particularly interleukin (IL)-17 and IL-22 in tears of patients with dry eye syndrome. Methods Tear samples were collected from 20 healthy volunteers, 20 dry eye (DE) patients with non-Sjö gren's syndrome (NSSDE) and 20 DE patients with Sjö gren's syndrome (SSDE). Symptom questionnaire was self-administered and multiple dry eye disease (DED)-related clinical tests were performed. The levels of IL-17 and IL-22 in tears were measured by enzyme-linked immunosorbent assay. Results The levels of IL-17 and IL-22 were significantly increased in tears of DE patients compared with those of controls and also higher in SSDE patients compared with those of NSSDE patients (Po0.05). Moreover, the levels of IL-17 and IL-22 were positively correlated with questionnaire score and keratopathy score but negatively correlated with tear film break-up time and Schirmer I test in both NSSDE and SSDE patients (Po0.05). Conclusions The levels of IL-17 and IL-22 in tears were significantly increased in DE patients, which were associated with the disease severity. Therefore, Th17 cellassociated cytokines, particularly IL-17 and IL-22, may have important roles in the immunopathogenesis of the DED.

Th17 cells are principal mediators of many autoimmune conditions. Recently, memory Th17 cells have been revealed as crucial in mediating the chronicity of various refractory autoimmune disorders; however, the underlying mechanisms maintaining memory Th17 cells have remained elusive. Here, using a preclinical model of ocular autoimmune disease we show that both IL-7 and IL-15 are critical for maintaining pathogenic memory Th17 cells. Neutralization of these cytokines leads to substantial reduction of memory Th17 cells; both IL-7 and IL-15 provide survival signals via activating STAT5, and IL-15 provides additional proliferation signals via activating both STAT5 and Akt. Topical neutralization of ocular IL-7 or IL-15 effectively reduces memory Th17 cells at the inflammatory site and draining lymphoid tissues, while topical neutralization of IL-17 alone, the major pathogenic cytokine secreted by Th17 cells, does not diminish memory Th17 cells at the draining lymphoid tissues. Our results suggest that the effective removal of pathogenic memory Th17 cells via abolishing environmental IL-7 or IL-15 is likely to be a novel strategy in the treatment of autoimmune diseases.

Super formula (LSF), and Emmetropia Verifying Optical formulas in highly myopic eyes.DESIGN: Retrospective, consecutive case-series study. METHODS: A total of 164 eyes of 164 patients with AL ‡26.0 mm were included and divided into 2 groups: AL <28.0 mm (Group 1) and AL ‡28.0 mm (Group 2). The average arithmetic spherical equivalent prediction error (PE), mean absolute PE, median absolute error (MedAE), and the percentage of eyes within ±0.25 diopter (D), ±0.50 D, and ±1.0 D of PE were determined. RESULTS: The Holladay 1 formulas showed the smallest MedAE when combined with the first linear or nonlinear version of Wang-Koch AL adjustment methods, both in total and in subgroups. The SRK/T formula displayed the highest prediction accuracy in combination with the first linear version of Wang-Koch adjustment method in total and subgroups. The CMAL reduced the absolute PE of LSF in total (P [ .003) and in Group 1 (P [ .017).CONCLUSIONS: The Holladay 1 and SRK/T formulas combined with specific AL adjustment methods had accuracy similar to the fourth-generation formulas for highly myopic eyes. Moreover, the CMAL can improve the accuracy of the LSF for highly myopic eyes.

Transforming growth factor β (TGFβ)-induced epithelial-mesenchymal transition (EMT) of lens epithelial cells (LECs) plays a key role in the pathogenesis of anterior subcapsular cataract (ASC) and capsule opacification. In mouse lens, Sprouty2 (Spry2) has a negative regulatory role on TGFβ signaling. However, the regulation of Spry2 during ASC development and how Spry2 modulates TGFβ signaling pathway in human LECs have not been characterized. Here, we demonstrate that Spry2 expression level is decreased in anterior capsule LECs of ASC patients. Spry2 negatively regulates TGFβ2-induced EMT and migration of LECs through inhibition of Smad2 and ERK1/2 phosphorylation. Also, blockade of Smad2 or ERK1/2 activation suppresses EMT caused by Spry2 downregulation. Collectively, our results for the first time show in human LECs that Spry2 has an inhibitory role in TGFβ signaling pathway. Our findings in human lens tissue and epithelial cells suggest that Spry2 may become a novel therapeutic target for the prevention and treatment of ASC and capsule opacification.

Capsular outcomes of anterior/posterior capsulorhexis opening (ACO/PCO) are essential for performing a secondary in-the-bag intraocular lens implantation. To compare the capsular outcomes with different primary capsulorhexis sizes, Thirty-eight eligible patients (45 eyes) were randomly assigned to three groups by anterior capsulorhexis diameter (Group A: 3.0–3.9, Group B: 4.0–5.0, and Group C: 5.1–6.0 mm). The areas of ACO/PCO and posterior capsule opening opacity (PCOO) as primary outcomes, while, the incidence of visual axis opacity (VAO) as secondary outcome were measured at follow-up visits. Among the thirty eyes included in the final analysis, the mean area of the ACO decreased significantly, whereas the PCO enlarged with time. Group A had the highest anterior capsule constriction and percentage reduction, which increased with time. There were significant differences in the percentage reductions at 6 months and 1 year compared to 1 month in Group A and B. Group C had the highest posterior capsule enlargement. The percentage of PCOO to PCO area and the incidence of VAO was highest in Group A and lowest in Group C. Thus, Capsulorhexis diameter of 4.0–5.0 mm may yield better capsular outcomes, considering moderate contraction of ACO, moderate enlargement of PCO, and lower percentage of PCOO and VAO.

Our study elucidates the function of epithelium-derived TSP-1 in inhibiting DC maturation and shows its translational potential to limit corneal epitheliopathy in DED.

Biocompatibility of intraocular lens (IOL) is critical to vision reconstruction after cataract surgery. Foldable hydrophobic acrylic IOL is vulnerable to the adhesion of extracellular matrix proteins and cells, leading to increased incidence of postoperative inflammation and capsule opacification. To increase IOL biocompatibility, we synthesized a hydrophilic copolymer P(MPC-MAA) and grafted the copolymer onto the surface of IOL through air plasma treatment. X-ray photoelectron spectroscopy, atomic force microscopy and static water contact angle were used to characterize chemical changes, topography and hydrophilicity of the IOL surface, respectively. Quartz crystal microbalance with dissipation (QCM-D) showed that P(MPC-MAA) modified IOLs were resistant to protein adsorption. Moreover, P(MPC-MAA) modification inhibited adhesion and proliferation of lens epithelial cells (LECs) in vitro. To analyze uveal and capsular biocompatibility in vivo, we implanted the P(MPC-MAA) modified IOLs into rabbits after phacoemulsification. P(MPC-MAA) modification significantly reduced postoperative inflammation and anterior capsule opacification (ACO), and did not affect posterior capsule opacification (PCO). Collectively, our study suggests that surface modification by P(MPC-MAA) can significantly improve uveal and capsular biocompatibility of hydrophobic acrylic IOL, which could potentially benefit patients with blood-aqueous barrier damage.

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